Gastric emptying and duodeno-gastro-oesophageal reflux in gastro-oesophageal reflux disease

BACKGROUND: Previous studies present conflicting results regarding relationship between gastric emptying and gastro-oesophageal reflux disease. Reflux of duodenal content to oesophagus is generally considered to be associated with more severe disease. AIM: To assess presence of a gastric emptying disorder in persons with reflux of duodenal contents to oesophagus and to identify any correlation with gastric emptying and oesophageal motility. METHODOLOGY: A total of 15 subjects with (B+) and 15 subjects without (B-) bile reflux to oesophagus determined by 24-hour bilirubin monitoring were studied with scintigraphic solid gastric emptying and 24-hour oesophageal manometry. RESULTS: There was no difference in lag phase [median 23.7 (range 10.8-44.0) vs 24.6 (8.1-40.1) min], half emptying time [74.6 (48.0-93.6) vs 82.8 (54.4-153.9) min] or emptying rate [0.89 (0.59-1.34) vs 0.83 (0.36-1. 15)%/min] for B- and B+ subjects, respectively. In addition, there was no difference in emptying rate of gastric fundus between B- and B+ subjects. Subjects with bile reflux had less effective oesophageal contractions of oesophageal body [9.4(3.3-37)%] compared to subjects without bile reflux [32(19-47)%, p = 0.002]. However, there was no correlation between oesophageal motility and gastric emptying. CONCLUSION: Results suggest that a gastric emptying disorder is a less likely contributing cause of bile reflux to the oesophagus, but bile reflux is associated with less effective oesophageal motility.     

Toxic bile acids in gastro-oesophageal reflux disease: influence of gastric acidity

BACKGROUND: Bile acid toxicity has been shown in the gastric, colonic, and hepatic tissues; the effect on oesophageal mucosa is less well known. AIMS: To determine the spectrum of bile acids refluxing in patients with gastro-oesophageal reflux disease and its relation to oesophageal pH using a new technique of combined oesophageal aspiration and pH monitoring. METHODS: Ten asymptomatic subjects and 30 patients with symptoms of gastro-oesophageal reflux disease (minimal mucosal injury, erosive oesophagitis (grade 2 or 3 Savary-Miller), Barrett's oesophagus/stricture; n=10 in each group) underwent 15 hour continuous oesophageal aspiration with simultaneous pH monitoring. Bile acid assay of the oesophageal samples was performed using modified high performance liquid chromatography. RESULTS: The peak bile acid concentration and DeMeester acid scores were significantly higher in the patients with oesophagitis (median bile acid concentration 124 micromol/l; acid score 20.2) and Barrett's oesophagus/stricture (181 micromol/l; 43. 3) than patients with minimal injury (14 micromol/l; 12.5) or controls (0 micromol/l; 11.1). The predominant bile acids detected were cholic, taurocholic, and glycocholic acids but there was a significantly greater proportion of secondary bile acids, deoxycholic and taurodeoxycholic acids, in patients with erosive oesophagitis and Barrett's oesophagus/stricture. Although bile acid reflux episodes occurred at variable pH, a temporal relation existed between reflux of taurine conjugates and oesophageal acid exposure (r=0.58, p=0.009). CONCLUSION: Toxic secondary bile acid fractions have been detected in patients with extensive mucosal damage. Mixed reflux is more harmful than acid reflux alone with possible toxic synergism existing between the taurine conjugates and acid.     

Does the addition of a prokinetic to proton pump inhibitor therapy help reduce duodenogastro-oesophageal reflux in patients with Barrett's oesophagus?

OBJECTIVE: The metaplastic change of Barrett's oesophagus is linked to both acid and duodenal reflux together with impaired motility. Proton pump inhibitors (PPI) reduce acid reflux, but no treatment is available that reduces duodenogastro-oesophageal reflux (DGOR). The aim of this study was to investigate whether adding a prokinetic to PPI treatment could improve oesophageal motility and subsequently reduce reflux. METHODS: Two groups of patients with Barrett's oesophagus on PPI therapy (prokinetic, n = 12; placebo, n = 11) were investigated. At visit 1, ambulatory oesophageal manometry was performed, and peristaltic and simultaneous wave percentage and characteristics were measured. DGOR and pH measurements were also performed. After treatment with either the prokinetic cisapride or placebo, all investigations were repeated (visit 2). Analysis of covariance and Spearman's correlation coefficients of changes from visit 1 to visit 2 were used to compare data. RESULTS: There was no significant difference between the two groups with respect to DGOR, DGOR characteristics, or the percentage of peristalsis and simultaneous waves and their characteristics. There was no correlation between DGOR and motility changes. Although no significant differences existed between acid reflux in the two groups, five patients with high supine acid reflux showed a significant reduction after treatment with cisapride. CONCLUSIONS: Addition of cisapride to PPI treatment does not appear to improve oesophageal motility or reduce DGOR in patients with Barrett's oesophagus.     

Oesophageal motor events at the occurrence of acid reflux and during endogenous acid exposure in healthy subjects and in patients with oesophagitis.

In order to assess the oesophageal motor events associated with the occurrence of gastro-oesophageal acid reflux and those during endogenous acid exposure, we studied six healthy subjects and nine patients with symptoms and lesions of reflux oesophagitis. In the case of each subject simultaneous pressure and pH measurements of the distal oesophagus were taken both in fasting conditions and after a standardised balanced meal. Reflux episodes occurred in the absence of a lower oesophageal sphincter relaxation (34.3%, 17.7%) or in the presence of a relaxation associated (34.2%, 30.8%) or unassociated (31.5%, 51.5%) with a peristaltic sequence, in the controls and patients respectively. No significant differences were found between the two groups. During endogenous acid perfusion the distal oesophagus showed mainly a peristaltic motor activity, but the mean hourly number of peristaltic sequences was significantly lower in the patients than in the controls (33.5 +/- 27.2 vs 81.5 +/- 3.2, p less than 0.01). Our results show that the mechanisms of reflux are similar in controls and in patients, while the peristaltic frequency is reduced in the latter. This motor failure may be responsible for the increased reflux duration observed in patients with oesophagitis.     

Role of acid and bile reflux in development of specialised intestinal metaplasia in distal oesophagus

BACKGROUND: Barrett's oesophagus is defined as specialised intestinal metaplasia in the distal oesophagus, regardless of extension. AIM: To study distal oesophagus function, and acid and bile exposure in patients with Long Segment (>3 cm), Short Segment (1 to 2 cm) and Ultra-short Segment (<1 cm) Barrett's Oesophagus, and in patients with gastro-oesophageal reflux disease without intestinal metaplasia. PATIENTS: Study population comprised 17 patients with Long, 8 with Short, 9 with Ultra-Short Segment Barrett's oesophagus, 32 with reflux disease and 12 healthy volunteers. METHODS: Patients were evaluated by manometry and by 24-hour pH and bile monitoring. RESULTS: Patients with intestinal metaplasia had greater acid exposure of the distal oesophagus than healthy volunteers. Patients with Long Segment Barrett's oesophagus had a longer history of symptoms, worse lower oesophageal sphincter pressures and longer bile and acid exposure than the other patients. Long Segment Barrett's oesophagus was predicted by low oesophageal pressure and increased bile exposure, age and male sex. CONCLUSION: Acid exposure in the distal oesophagus is probably the aetiological factor behind intestinal metaplasia, but a severely damaged antireflux barrier and bile in the refluxate are necessary for Long Segment Barrett's Oesophagus to develop.     

Primary peristalsis is the major acid clearance mechanism in reflux patients.

This study examined the clearance of gastric acid from the oesophagus in ambulant patients with gastro-oesophageal reflux. Eighteen patients with proved reflux disease were studied, nine with (group 1) and nine without (group 2) endoscopic oesophagitis. Oesophageal pressure and pH were recorded over 24 hours. Pressures were measured by a probe with five sensors: a 5 cm long sensor in the lower oesophageal sphincter, three sensors in the body of the oesophagus, and one at the pharynx to detect swallowing. Oesophageal pH was monitored 5 cm above the lower oesophageal sphincter. Manometric activities were classified as either peristaltic or ineffective. The latter included simultaneous, non-transmitted, and low amplitude peristaltic contractions. A reflux episode was defined as starting when pH fell to less than 4 and ending when the pH rose to 5. When the rise to pH 5 took place in three or more discrete steps after motor responses to gastro-oesophageal reflux, the pH steps were labelled as initial change (I), middle changes (M), and last change (L). A total of 595 episodes of gastro-oesophageal reflux and 1626 associated motor events were analysed. Of these, 1331 (81.9%) were classed as primary peristaltic activity, 174 (10.7%) as primary ineffective activity, 46 (2.8%) as secondary peristaltic activity, and 75 (4.6%) as secondary ineffective activity. There were no significant differences in initial change (p > 0.05), middle changes (p > 0.05), and last change (p > 0.05) between group 1 and group 2. In all patients, the successive changes of pH in response to motor activity were significantly different (p = 0.0001) between initial, middle, and last changes. Last change was significantly higher when compared with initial (p=0.001) and middle changes (p<0.001). Primary oesophageal peristalsis was the most frequent motor response to gastro-oesophageal reflux. The last motor activity during reflux showed the greatest change in pH.     

Effects of intraluminal acidification on oesophageal motor activity.

This study assessed the effect of prolonged intraluminal acidification on the motor activity of the entire oesophageal body (under controlled conditions). Intraoesophageal pressures were recorded in 13 endoscopy negative subjects with gastro-oesophageal reflux disease in whom saline, HC1 0.1 N, and saline solutions were infused (1.5 ml/min) blindly in the oesophageal body, 6 cm distal to the upper oesophageal sphincter for three consecutive periods of 45 minutes each. These findings were compared with those of a control group. Intraoesophageal acidification caused an increase in the deglutition frequency (p < 0.02), the occurrence of multipeaked waves (p < 0.04) as well as a decrease of the propagating velocity (p < 0.04) of the primary peristaltic contractions. Furthermore, intraoesophageal acidification determined an increase, at all levels of the oesophagus, of the duration (p < 0.04) and, more noticeable in the proximal oesophageal body, of the amplitude (p < 0.02) of primary peristaltic contraction waves. In conclusion prolonged intraoesophageal acidification can considerably affect frequency of deglutition, morphology, and propagating patterns of primary peristaltic contractions. This study shows that these effects are independent from volume distension of the oesophagus and supports the presence of acid sensitive receptors in the oesophageal mucosa.     

Bile reflux and oesophagitis

Duodenal contents, and especially bile acids and trypsin, are noxious to the oesophageal mucosa, their damaging potential depending on pH. Various methodologies have been used to measure duodenogastric or duodenogastro-oesophageal reflux, all of them having technical limitations. Controversy exists as to the extent of duodenogastric reflux in GORD. Reflux of both acid and duodenal contents into the oesophagus increases with worsening of oesophagitis. Experimental data suggest that bile acids and trypsin are noxious to the oesophageal mucosa and that their damaging potential depends on pH. The injurious concentrations are, however, higher than those usually observed in the human oesophagus. Direct measurement of bile acids and trypsin is difficult and various methodologies have been used to measure duodenogastric or duodenogastro-oesophageal reflux, all of them having technical limitations. Whereas available data as to the extent of duodenogastric reflux in gastro-oesophageal reflux disease (GORD) are controversial, most observations show that reflux of both acid and duodenal contents into the oesophagus increases with worsening of oesophagitis. Furthermore, acid and duodenal contents occur simultaneously in most reflux episodes. In this issue of the journal, Marshall et al. report that exposure of the gastric fundus to duodenal contents as assessed by bilirubin monitoring is similar in GORD patients with varying degrees of oesophageal mucosal injury and in healthy controls.     

High amplitude contractions in the middle third of the oesophagus: a manometric marker of chronic alcoholism?

BACKGROUND--Oesophageal motor abnormalities have been reported in alcoholism. AIM--To investigate the effects of chronic alcoholism and its withdrawal on oesophageal disease. PATIENTS--23 chronic alcoholic patients (20 men and three women; mean age 43, range 23 to 54). METHODS--Endoscopy, manometry, and 24 hour pH monitoring 7-10 days and six months after ethanol withdrawal. Tests for autonomic and peripheral neuropathy were also performed. Motility and pH tracings were compared with those of age and sex matched control groups: healthy volunteers, nutcracker oesophagus, and gastro-oesophageal reflux disease. RESULTS--14 (61%) alcoholic patients had reflux symptoms, and endoscopy with biopsy showed oesophageal inflammation in 10 patients. One patient had an asymptomatic squamous cell carcinoma. Oesophageal motility studies in the alcoholic patients showed that peristaltic amplitude in the middle third was > 150 mm Hg (95th percentile (P95) of healthy controls) in 13 (57%), the ratio lower/ middle amplitude was < 0.9 in 15 (65%) (> 0.9 in all control groups), and the lower oesophageal sphincter was hypertensive (> 23.4 mm Hg, P95 of healthy controls) in 13 (57%). All three abnormalities were present in five (22%). Abnormal reflux (per cent reflux time > 2.9, P95 of healthy controls) was shown in 12 (52%) alcoholic patients, and was unrelated to peristaltic dysfunction. Subclinical neuropathy in 10 patients did not effect oesophageal abnormalities. Oesophageal motility abnormalities persisted at six months in six patients with ongoing alcoholism, whereas they reverted towards normal in 13 who remained abstinent; reflux, however, was unaffected. CONCLUSIONS--Oesophageal peristaltic dysfunction and reflux are frequent in alcoholism. High amplitude contractions in the middle third of the oesophagus seem to be a marker of excessive alcohol consumption, and tend to improve with abstinence.     

Oesophageal function in patients with angina pectoris: a comparison of patients with normal coronary angiograms and patients with coronary artery disease

Oesophageal function was assessed in 52 patients with angina pectoris whose coronary angiograms were completely normal and in 21 patients with angina pectoris who had significant coronary artery disease. During a standard oesophageal manometric study, abnormalities were found in 23 (44%) patients with normal coronary angiograms but in only 2 (10%) patients with coronary artery disease (p less than 0.01). Twenty-four (46%) patients with normal coronary angiograms were found to have gastro-oesophageal reflux disease during 24-hour oesophageal pH monitoring. Of the 52 patients with normal coronary angiograms, 19 (37%) had gastro-oesophageal reflux disease and abnormal oesophageal motility, 5 (10%) had gastro-oesophageal reflux disease alone, and 7 (13%) had oesophageal motility disorder alone. The use of provocation procedures, including intravenous edrophonium during oesophageal manometry and treadmill exercise testing during pH monitoring, enabled the oesophageal abnormality to be demonstrated simultaneously with chest pain in 25 of these 31 patients. Typical angina pectoris, coincident with abnormal oesophageal motility, was precipitated in a subgroup of patients who had been shown to have oesophageal manometric abnormalities and gastro-oesophageal reflux disease by the infusion of hydrochloric acid into the oesophagus; both the chest pain and manometric abnormality resolved following the oral administration of antacid.     

Intra-oesophageal acid suppression in complicated gastro-oesophageal reflux disease: esomeprazole versus lansoprazole

BACKGROUND: Acid suppression is the mainstay of therapy in gastro-oesophageal reflux disease. Esomeprazole 40 mg is more effective than lansoprazole 30 mg in healing mucosal lesions in severe erosive reflux oesophagitis. However, data comparing esomeprazole with lansoprazole in patients with complications of gastro-oesophageal reflux disease, such as ulcerative reflux oesophagitis and Barrett's oesophagus, are lacking. AIM: To compare the efficacy of esomeprazole and lansoprazole at their standard dosages in suppressing oesophageal acid exposure in complicated gastro-oesophageal reflux disease. METHODS: Thirty patients with complicated gastro-oesophageal reflux disease (7 with ulcerative reflux oesophagitis and 23 with Barrett's oesophagus), randomly assigned to receive 40 mg esomeprazole (n=16) or 30 mg lansoprazole (n=14) once daily, underwent oesophageal 24-h pH monitoring while on therapy. Total, upright diurnal and supine nocturnal percentage acid reflux time were assessed. RESULTS: Esomeprazole was significantly more effective than lansoprazole in decreasing oesophageal acid exposure. Normalisation of both total and supine nocturnal percentage acid reflux time was obtained in 12 of 16 (75%) patients treated with esomeprazole but only in 4 of 14 (28%) cases treated with lansoprazole (p=0.026). CONCLUSIONS: Normalisation of oesophageal acid exposure can be achieved in the majority of complicated gastro-oesophageal reflux disease cases with esomeprazole 40 mg once daily.     

Primary oesophageal motility disorders: how primary are they?

The normal regulation of oesophageal peristalsis is complex. Nitric oxide-containing inhibitory neurons and cholinergic excitatory nerve fibres play the key roles. In the so-called primary oesophageal motility disorders, the coordination of oesophageal contractions and lower oesophageal sphincter function is disturbed (achalasia, diffuse oesophageal spasm), or the amplitudes of peristaltic contractions are abnormally high (nutcracker oesophagus). This article focuses on the pathophysiology of achalasia and nutcracker oesophagus. There is evidence that achalasia and nutcracker oesophagus should not be considered parts of one and the same range of diseases.     

Acid clearance and oesophageal sensitivity in patients with progressive systemic sclerosis.

This study examined the hypothesis that impaired oesophageal peristalsis was associated with delayed oesophageal clearance of acid in patients with progressive systemic sclerosis (PSS), some of whom are thought to have impaired oesophageal sensitivity to acid. Sixteen patients with PSS had: (a) oesophageal manometry and endoscopy; (b) acid perfusion of the oesophagus with simultaneous measurement of intraoesophageal pH during perfusion and for the next 10 minutes; (c) 22 hour monitoring of intraoesophageal pH; and (d) an evaluation of reflux symptoms during and after perfusion and during overnight pH monitoring. By oesophageal manometry, eight patients had normal peristalsis and eight patients had impaired peristalsis. Oesophageal endoscopy was unremarkable in patients with normal peristalsis, whereas all patients with impaired peristalsis had oesophagitis. The time needed to clear the oesophagus of perfused acid was shorter (p < 0.01) in patients with normal peristalsis and acid clearance time was significantly correlated (p < 0.01) with acid exposure time during overnight pH monitoring. During and after oesophageal perfusion, the nature, duration, and severity of symptoms did not differ between the groups, but overnight symptoms lasted longer (p < 0.05) in patients with impaired peristalsis. It is concluded that in PSS: (1) Impaired oesophageal motility delayed the clearance of acid and increased the exposure time to acid. (2) Acid clearance time is a useful parameter of impaired oesophageal motor function. The assessment of acid clearance time can be used as an alternative to overnight pH monitoring, to assess the impairment of oesophageal acid clearance. (3) Oesophageal sensitivity to acid was preserved in patients with impaired peristalsis and oesophagitis. (4) Reflux symptoms lasted longer in patients with prolonged oesophageal acid exposure but were still reported for a small fraction of the total acid exposure time. Thus, reflux symptoms reflect poorly prolonged exposure of the oesophagus to acid and are not a reliable guide to acid injury of the oesophagus in PSS.     

Is ineffective oesophageal motility associated with reflux oesophagitis?

OBJECTIVE: To evaluate the association between ineffective oesophageal motility and reflux oesophagitis controlling for hiatal hernia, hypotensive lower oesophageal sphincter and male sex in patients with gastro-oesophageal reflux disease. METHODS: A total of 387 patients with reflux disease (mean age, 46 years, 42% men) were consecutively selected from a database. All patients underwent upper endoscopy, oesophageal manometry and 24 h oesophageal pH-metry in accordance with a standardized protocol. Reflux disease was confirmed either by endoscopy (oesophagitis grade I-IV according to Savary-Miller) or by pH-metry (increased acid exposure). Hiatal hernia was diagnosed endoscopically, whereas ineffective oesophageal motility and hypotensive lower oesophageal sphincter were characterized during manometry testing. The association between ineffective oesophageal motility and reflux oesophagitis was assessed by logistic regression analysis. RESULTS: A total of 166 patients with oesophagitis (mean age 45 years, 49% men) and 221 without oesophagitis (mean age 46 years, 37% men) were present. Prevalences of ineffective oesophageal motility, hiatal hernia, hypotensive lower oesophageal sphincter and male sex were significantly higher in patients with oesophagitis compared with those without oesophagitis (P<0.05). Ineffective oesophageal motility was independently associated with oesophagitis after multivariate logistic regression analysis (odds ratio=1.68; 95% confidence interval=1.04-2.70). CONCLUSION: Ineffective oesophageal motility is associated with reflux oesophagitis, independently of hiatal hernia, hypotensive lower oesophageal sphincter and male sex.     

Composition of gastro-oesophageal refluxate.

Fifty two patients with abnormal acid gastro-oesophageal reflux were studied by simultaneous oesophageal pH monitoring and continuous aspiration for 16 hours. Aspirates (from discrete two hour periods) were analysed for volume, pH, bile acids (conjugated and unconjugated), trypsin, and pepsin. The results were compared with pH changes and degree of oesophagitis. Patients with oesophagitis had greater acid reflux than those without, but patients with stricture and Barrett's oesophagus had similar acid reflux to those with uncomplicated erosive oesophagitis. Pepsin concentrations were highest in patients with stricture and Barrett's oesophagus particularly during nocturnal periods. Conjugated bile acids were detected in 75% of patients, mainly during the night, but only 2% of aspirates contained concentrations likely to be cytotoxic. Unconjugated bile acids were not detected, and trypsin was seldom found. Reflux oesophagitis is caused by acid and pepsin. Bile acids and trypsin are probably unimportant.     

Reflux-associated nutcracker oesophagus in a 49-year-old patient with non-cardiac chest pain (NCCP)

A 49-year-old woman was admitted to our department because of intermittent left-sided chest pain for the past 2 years. The patient reported an increasing frequency and duration of the symptoms which were independent from food intake, medication or physical exercises. A cardiac cause of the chest pain was excluded before admittance to our hospital. The initially performed upper endoscopy revealed a small oesophageal hiatal hernia but no signs of acute or chronic inflammation. Basal oesophageal manometry and pH monitoring confirmed the presence of a nutcracker oesophagus, defined by high-amplitude contractions of the distal oesophagus, in combination with a gastro-oesophageal reflux disease. The patient was treated with high-dose pantoprazole for 8 weeks before re-examination. Interestingly, the symptoms completely disappeared upon medication and the relief of the chest pain was accompanied by normalisation of the nutcracker oesophagus pattern. Thus, our observation provides evidence for a causative role of acid reflux in the pathophysiology of the nutcracker oesophagus and, in addition, suggests that effective acid suppression might be a useful therapeutic tool to deal with this painful motility disorder of the oesophagus.     

Does oesophageal motor function improve with time after successful antireflux surgery? Results of a prospective,randomised clinical study.

MAIN OBJECTIVE: There is a continuing debate whether motor abnormalities associated with gastro-oesophageal reflux disease (GORD) are primary phenomena or occur as a consequence of repeated injury caused by inflammation. To get new insights into mechanisms involved, patients were studied before and three years after effective and durable reflux control induced by two types of fundoplications. PATIENTS AND METHODS: Thirty three consecutive patients with chronic GORD entered the trial. All patients had a clinical history of GORD assessed symptomatically, endoscopically, and by use of 24 hour pH-metry. Eighteen were randomised to a 180 degrees semifundoplication (Toupet) and 15 to a total fundic wrap (Nissen-Rossetti). Manometry was done preoperatively, six months, and three years after the operation assessing motor function in defined areas of the tubular oesophagus and lower oesophageal sphincter. RESULTS: All patients had a proper control of GORD both when objectively and clinically assessed. Postoperatively, the resting tone of the lower oesophageal sphincter was significantly higher in the Nissen-Rossetti group (p < 0.05), and the intra-abdominal portion of the lower oesophageal sphincter was of identical length in the two groups. A significant increase in peristaltic amplitude in the middle and distal third of the oesophagus was recorded at long term follow up compared with the preoperative findings (p < 0.05), but there was no corresponding effect on propagation speed and duration of contraction. However, an increase in peristaltic amplitude and, as a tentative consequence, a significant decrease (p < 0.05) in the frequency of primary peristalsis was found only in patients operated on with a total fundic wrap. CONCLUSION: Despite adequate and durable reflux control after fundoplication in patients with chronic GORD, no change was found in oesophageal motor function with time. The higher contraction amplitude and decreased frequency of failed primary peristalsis seen in patients having a total fundic wrap were thus most likely due to a mechanical outflow obstruction in the gastro-oesophageal junction. These results could therefore be interpreted in favour of the hypothesis that GORD is pathogenetically linked to a primary defect in oesophageal motor function.     

Effect of coffee on gastro-oesophageal reflux in patients with reflux disease and healthy controls

BACKGROUND: Many patients with gastro-oesophageal reflux disease (GORD) report that coffee aggravates their symptoms and doctors tend to discourage its use in GORD. OBJECTIVE: To assess the effect of coffee ingestion on gastro-oesophageal acid reflux. DESIGN: A randomized, controlled, crossover study. PARTICIPANTS: Seven GORD patients and eight healthy subjects. METHODS: After 1 day of coffee abstinence, participants underwent 24-h oesophageal pH and manometric monitoring. At well-defined times, they ingested either 280 ml of regular paper-filtered coffee or 280 ml of warm water. Coffee or water was drunk 1 h after breakfast, during lunch, 1 h after dinner and after an overnight fast Reflux and oesophageal motility parameters were assessed for the first hour after each coffee or water intake. RESULTS: Coffee had no effect on postprandial acid reflux time or number of reflux episodes, either in GORD patients or in healthy subjects. Coffee increased the percentage acid reflux time only when ingested in the fasting period in the GORD patients (median 2.6, range 0-19.3 versus median 0, range 0-8.3; P = 0.028), but not in the healthy subjects. No effect of coffee on postprandial lower oesophageal sphincter pressure (LOSP), patterns of LOSP associated with reflux episodes or oesophageal contractions was found. CONCLUSION: Coffee has no important effect on gastro-oesophageal acid reflux in GORD patients, and no effect at all in healthy subjects.     

Gastroesophageal reflux and chronic cough

Gastroesophageal reflux (GOR) disease is one of the 3 commonest causes of chronic cough. It can be difficult to diagnose as the traditionally recognised symptoms of GOR, such as heartburn and acid regurgitation, are often absent. More subtle indicators of a link between the cough and the oesophagus should therefore be sought. These include cough which occurs in relation to eating or phonation, cough which settles at night and does not tend to wake the patient from sleep and symptoms suggestive of laryngopharyngeal reflux. Investigations such as oesophageal manometry and 24 hour pH monitoring can be useful in characterising any underlying oesophageal abnormality, but may underestimate the problem since non-acid reflux can precipitate cough. Empirical trials of treatment are therefore often employed, but should be continued for at least 2 months, as symptoms can be slow to improve due to plasticity of the cough reflex. Pharmacologic treatment options include proton pump inhibitors, H2 receptor antagonists, pro-motility agents and liquid alginate preparations. Surgical fundoplication can also be effective when performed in appropriately selected individuals.     

Fate of Nissen fundoplication after 20 years. A clinical, endoscopical, and functional analysis.

Of 46 patients who had Nissen fundoplication for proved gastro-oesophageal reflux, 25 were available for follow up after a median of 20 years, 15 had died of unrelated causes, and six could not be traced. All 25 patients in the follow up study were personally interviewed: 21 consented to an endoscopy, 14 to 24 hour recording of oesophageal pH and manometry, and 15 to radionuclide transit test. Repeat fundoplication for recurrent reflux was performed in two cases during the study. Heartburn and regurgitation were significantly lessened (p < 0.005), but the incidence of dysphagia was slightly increased. Endoscopy showed six of 21 fundic wraps to be defective. Erosive oesophagitis was seen in two patients, and Barrett's oesophagus (histologically confirmed) in one of them and six other patients. Total reflux time was abnormal in four of 14 patients. No patient with an intact fundic wrap seen on endoscopy, only two of seven with Barrett's oesophagus, and one of four with abnormal reflux had oesophagitis. Fundoplication in itself did not affect oesophageal motility or transit, provided that the wrap was intact. It is concluded that Nissen fundoplication gave a reasonably good longterm effect in chronic reflux disease, with the stage of the fundic wrap as the main determinant of outcome.